The RAB25 small GTPase determines aggressiveness of ovarian and breast cancers

Authors:
Cheng KW, Lahad JP, Kuo WL, Lapuk A, Yamada K, Auersperg N, Liu J, Smith-McCune K, Lu KH, Fishman D, Gray JW and Mills GB
In:
Source: Nat Med
Publication Date: (2004)
Issue: 10(11): 1251-1256
Research Area:
Cancer Research/Cell Biology
Cells used in publication:
OVCAR3
Species: human
Tissue Origin: ovarian
A2780
Species: human
Tissue Origin: ovarian
Platform:
Nucleofector® I/II/2b
Experiment
The human ovarian carcinoma cell lines A2780 and OVCAR3, and the human breast carcinoma cell line MCF-7 were transfected with control or RAB25 siRNA.
Abstract
High-density array comparative genomic hybridization (CGH) showed amplification of chromosome 1q22 centered on the RAB25 small GTPase, which is implicated in apical vesicle trafficking, in approximately half of ovarian and breast cancers. RAB25 mRNA levels were selectively increased in stage III and IV serous epithelial ovarian cancers compared to other genes within the amplified region, implicating RAB25 as a driving event in the development of the amplicon. Increased DNA copy number or RNA level of RAB25 was associated with markedly decreased disease-free survival or overall survival in ovarian and breast cancers, respectively. Forced expression of RAB25 markedly increased anchorage-dependent and anchorage-independent cell proliferation, prevented apoptosis and anoikis, including that induced by chemotherapy, and increased aggressiveness of cancer cells in vivo. The inhibition of apoptosis was associated with a decrease in expression of the proapoptotic molecules, BAK and BAX, and activation of the antiapoptotic phosphatidylinositol 3 kinase (PI3K) and AKT pathway, providing potential mechanisms for the effects of RAB25 on tumor aggressiveness. Overall, these studies implicate RAB25, and thus the RAB family of small G proteins, in aggressiveness of epithelial cancers.